Blocking ETB receptors causes salt-sensitive hypertension and an increase in ET-1 plasma and urine levels. ET-1 also has been demonstrated to stimulate superoxide and to promote TxA2 synthesis through the ETA receptor. Blockade of the ETA receptor will prevent the hypertension produced by chronic ETB blockade, but the mechanism is not completely understood. The overall hypothesis is superoxide and thromboxane contributes to the pathophysiological effects of ETB receptor blockade in rats on a high salt diet. Specific Aims: 1. To test the hypothesis that superoxide contributes to the hypertension produced by ETB receptor blockade. 2. To test the hypothesis that TP receptor activation contributes to the hypertension produced by ETB receptor blockade. 3. To test the hypothesis that cortical blood flow and medullary blood flow is decreased in rats treated with an ETB receptor antagonist along with ET-1 infusion through the stimulation of TxA2 and superoxide acutely.